Rubinsztein David C, DiFiglia Marian, Heintz Nathaniel, Nixon Ralph A, Qin Zheng-Hong, Ravikumar Brinda, Stefanis Leonidas, Tolkovsky Aviva
Departments of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge, UK.
Autophagy. 2005 Apr;1(1):11-22. doi: 10.4161/auto.1.1.1513. Epub 2005 Apr 30.
Increased numbers of autophagosomes/autophagic vacuoles are seen in a variety of physiological and pathological states in the nervous system. In many cases, it is unclear if this phenomenon is the result of increased autophagic activity or decreased autophagosome-lysosome fusion. The functional significance of autophagy and its relationship to cell death in the nervous system is also poorly understood. In this review, we have considered these issues in the context of acute neuronal injury and a range of chronic neurodegenerative conditions, including the Lurcher mouse, Alzheimer's, Parkinson's, Huntington's and prion diseases. While many issues remain unresolved, these conditions raise the possibility that autophagy can have either deleterious or protective effects depending on the specific situation and stage in the pathological process.
在神经系统的各种生理和病理状态下,均可观察到自噬体/自噬泡数量增加。在许多情况下,尚不清楚这种现象是自噬活性增强还是自噬体-溶酶体融合减少的结果。自噬在神经系统中的功能意义及其与细胞死亡的关系也知之甚少。在本综述中,我们在急性神经元损伤和一系列慢性神经退行性疾病的背景下考虑了这些问题,包括Lurcher小鼠、阿尔茨海默病、帕金森病、亨廷顿病和朊病毒病。虽然许多问题仍未解决,但这些疾病增加了一种可能性,即根据病理过程中的具体情况和阶段,自噬可能具有有害或保护作用。